Development of an sRNA-mediated conditional knockdown system for .

We describe a new protein depletion method that uses an engineered small RNA (sRNA) to inhibit translation of a target gene. In proof-of-principle experiments, we induced functional knockdown of IncA, a fusion-mediating inclusion membrane protein, as shown with Western blots, loss of IncA staining at the inclusion membrane, and production of multiple chlamydial inclusions within an infected cell. These effects were titratable and reversible.

RNA Secondary Structure Mediates Staufen2 RNP Assembly in Neurons.

RNA-binding proteins (RBPs) act as posttranscriptional regulators controlling the fate of target mRNAs. Unraveling how RNAs are recognized by RBPs and in turn are assembled into neuronal RNA granules is therefore key to understanding the underlying mechanism. While RNA sequence elements have been extensively characterized, the functional impact of RNA secondary structures is only recently being explored.

Synergistic regulation of mRNA by HuR and miR-26/RISC in neurons.

The negative regulator of G-protein signalling 4 (Rgs4) is linked to several neurologic diseases, . schizophrenia, addiction, seizure and pain perception. Consequently, Rgs4 expression is tightly regulated, resulting in high mRNA and protein turnover.

Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1.

Macrophages play a dynamic role in tissue repair following injury. Here we found that following streptozotocin (STZ)-induced beta-cell death, mouse islet macrophages had increased Igf1 expression, decreased proinflammatory cytokine expression, and transcriptome changes consistent with macrophages undergoing efferocytosis and having an enhanced state of metabolism. Macrophages were the major, if not sole, contributors to islet insulin-like growth factor-1 (IGF-1) production.